1. CLINICAL MANIFESTATIONS OF ETHANOL INTOXICATION

2. It is unusual for persons with alcoholism to present for acute care with intoxication as their only medical problem Only 26% of patients intoxicated with ethanol had intoxication as their sole problem 116 motor vehicle accident admissions to an urban trauma service 53% had BECs greater than 100 mg%

3. Alcohol poisoning Arman Otroshi Forensic medicine & clinical toxicology

4. 50% of 289 patients with positive ethanol screens had at least one other drug toxic dose: 5 g/kg in an adult or 3 g/kg in a child BEC 25 mg% in the average adult: One ounce of whiskey (80 proof, or 40%), 12 ounces of beer, or 4 ounces of wine

5. The majority of states in the United States use 80 mg% as the legal limit for ethanol

6. Symptoms of intoxication begin with a perception of stimulation due to the suppression of central inhibitory mechanisms While BECs typically correlate with symptoms in nondrinkers chronic drinkers require higher levels to reach similar states of intoxication

7. signs and symptoms consistent with ethanol intoxication that include flushed facies, diaphoresis, tachycardia, hypotension, hypothermia, hypoventilation, mydriasis, nystagmus, vomiting, dysarthria, muscular incoordination, ataxia, altered consciousness, and coma

10. low doses: CNS depressant high doses: general depressant animated behavior and the loss of restraint: Cortical release Disinhibition causes paradoxical CNS stimulation

11. The degree of intoxication also correlates with the rate of rise of the BEC. Slower ethanol ingestion results in less intoxication.

12. mild intoxication energized and loquacious, expansive, emotionally labile, and increasingly gregarious lost self-control, exhibit antisocial behavior, and be ill-tempered

13. As the degree of intoxication increases successive inhibition and impairment of neuronal activity irritable, abusive, aggressive, violent, dysarthric confused, disoriented, or lethargic

14. With severe intoxication loss of airway protective reflexes, Coma: usually BEC >250 mg/dL (54.35 mmol/L) increasing risk of death from respiratory depression

15. acute effects of ethanol ingestion depend on habituation – mainly a result of the development of tolerance Metabolic tolerance – enhanced elimination by the ADH enzyme and CYP2E1 system Functional tolerance – more important, alterations in serotonergic and adrenergic neurons

16. Acute alcohol tolerance comparison of physiologic responses or behavioral effects at the same blood ethanol concentration on the ascending and descending limbs of the blood ethanol curve Impairment is greater at a given blood ethanol concentration when the blood ethanol concentration is increasing, than for the same blood ethanol concentration when the blood ethanol concentration is falling.

17. Inebriated patient A meticulous and systematic approach to the evaluation and management of an inebriated patient will help the clinician avoid potential pitfalls in such a situation

18. Inebriated patient presence or absence of an odor of ethanol on the breath: unreliable means Diplopia, visual disturbances, and nystagmus : toxic effects of ethanol or Wernicke encephalopathy Hypothermia may be – ethanol-induced vasodilation – exacerbated by environmental exposure – malnutrition and loss of carbohydrate or energy substrate

19. impair cardiac output in patients with preexisting cardiac disease atrial fibrillation and nonsustained ventricular tachycardia, atrioventricular block: binge drinkers

20. holiday heart syndrome supraventricular tachydysrhythmias in apparently healthy people heavy ethanol consumption binge, but who usually drink little ethanol most common dysrhythmia is atrial fibrillation, which usually reverts to normal sinus rhythm within 24 hours

21. holiday heart syndrome the clinical course is benign in patients without anatomic cardiac pathology, but recur antidysrhythmic therapy is usually not warranted

22. holiday heart syndrome Acute heavy ethanol drinking may precipitate silent myocardial ischemia in patients with stable angina pectoris

23. Acute altered mental status

24. differential diagnosis hypoglycemia, hypoxia, intracranial pathology, seizure, encephalopathy, uremia, cerebral infection, and shock Many medications cause an alteration in mental status including sedative-hypnotics, opioids, antidepressants, and antipsychotics.

25. Acute altered mental status acute ethanol or toxic ethanol intoxication; hypoglycemia; therapeutic or illicit drug overdose; Wernicke-Korsakoff syndrome; head trauma; a postictal condition; infection; an intracranial hematoma (acute or chronic); hepatic encephalopathy; an electrolyte or acid base disorder; or ethanol withdrawal

26. Ethanol-induced seizures reported in adults, but are more frequent in children

27. CLINICAL MANIFESTATIONS OF METHANOL INTOXICATION

28. Symptoms of methanol poisoning may be delayed for 12 to 24 hours, or even longer if ethanol is also ingested: – before – concomitantly – just after methanol consumption slow metabolism of methanol to the principal toxic product, formic acid

29. Symptoms of methanol poisoning methanol does not cause significant CNS depression and ethanol-like inebriation Early clinical features are nausea, vomiting, and abdominal pain, but these are also seen in later stages A few cases may also present as acute abdomen, probably cause of pancreatitis

30. Symptoms of methanol poisoning Clinical features of systemic toxicity : anorexia, headache, nausea, accompanied or followed by increasing hyperventilation The first complaint may often be shortness of breath because of hyperventilation chest pain and may therefore be admitted acutely with the diagnosis of acute myocardial infarction

31. Symptoms of methanol poisoning Visual symptoms (of all kinds, such as blind spots, blurred vision, or “snow fields”) may appear first, or with the symptoms above Usually ocular symptoms precede objective signs, such as dilated pupils that are partially reactive or nonreactive to light and fundoscopy showing optic disc hyperemia with blurring of the margins (pseudopapillitis)

32. Signs of methanol poisoning The blurring of the disc margin may look like papillary edema, but there is no diopter difference between the fundus and the disc

34. coma and respiratory and circulatory failure – If treatment is not initiated at early stage of poisoning Respiratory arrest – is a dramatic complication associated with a mortality rate of 75%

35. toxic effect on basal ganglia may not be evident in the acute stage because it is concealed by pronounced CNS depression. Survivors may later manifest a parkinsonian- like syndrome

40. Diagnose methanol poisoning is difficult to diagnose – In the absence of an exposure history – especially if ethanol is coingested and the latency period is prolonged. Therefore, methanol poisoning should be considered in every patient presenting with a metabolic acidosis of unknown origin

41. Diagnose Methanol – is usually determined by gas chromatography or radioimmunoassay techniques. Formate – usually not available in the clinical setting, but a recent simple enzymatic method has proven

42. Diagnose arterial blood gas analysis in addition to standard blood samples. If ethylene glycol poisoning is considered a differential diagnosis, urinalysis including microscopy should be performed in search of crystalluria. The presence of crystals may suggest ethylene glycol, although their absence has no diagnostic value.

43. physical examination focus on vital signs (especially respiratory rate). Visual acuity and fundoscopy examinations should be performed. The objective signs of ocular toxicity of methanol include dilated pupils, which are partially reactive or nonreactive to light, and optic disc hyperemia with blurring of the disc margins (pseudopapillitis)

44. hyperemia turns into pallor, which is usually associated with blindness

45. patient presents with a metabolic acidosis of unknown origin diabetic ketoacidosis and renal failure are ruled out anion and osmolal gaps should be calculated as a clue to the diagnosis ([Na + + K + ] – [Cl − + HCO 3 − ]) 12 ± 8 mmol/L accumulation of formate causes a metabolic acidosis with an increased anion gap

46. Diagnose In concentrations associated with toxicity, methanol also increases the serum osmolality, as do other alcohols 5 ± 14 mOsm/kg H 2 O decision level or cutoff value for the osmolal gap of 25 mOsm/kg H 2 O works very well

50. ETHYLENE GLYCOL POISONING

51. Presentation of patients is polymorphous, depending on the: – delay since ingestion – ingested dose – coingestion of ethanol – timing of medical intervention

53. Early after ingestion: – usually asymptomatic or only hyperventilation – Kussmaul's respiration – underestimation of poisoning severity may occur late presentation: – life-threatening signs and symptoms – coma, seizures, respiratory distress, renal failure

54. three classical theoretical stages onset and progression of this condition are not always straightforward or predictable

55. The first phase called neurologic occurs within 30 minutes to 12 hours after ingestion. Patients appear inebriated and euphoric, but without the characteristic alcohol smell. Nausea, vomiting, and hematemesis are possible, reflecting ethylene glycol gastrointestinal direct irritation

56. The first phase initial latent period: is not uncommon Rapidly, the most severely intoxicated patients may develop coma, myoclonic seizures, nystagmus, ataxia, ocular external muscle paralysis, CNS depression, and meningismus Cranial ct scans are usually normal diffuse cerebral edema, intraparenchymal hemorrhage or petechiae, and reversible hypodense areas localized in various brain, brainstem, and cerebellum territories

57. The second phase called cardiopulmonary starts between 12 and 24 hours after the ingestion. tachycardia, mild hypertension, pulmonary edema, ARDS, and CHF

58. The second phase calcium oxalate crystal deposition within the vascular tree, the myocardium, and the lung parenchyma Hypoxia may be related to aspiration pneumonia or CNS depression Dysrhythmias with QTc interval prolongation may be the consequence of profound hypocalcemia

59. The third phase called renal begins between 24 and 72 hours after the ingestion Patients present with flank pain and tenderness, oliguria, and ARF Bone marrow suppression has been reported, but hepatic damage is usually minimal Calcium oxalate or hippurate crystals are present in the urine

61. Delayed symptoms persistent renal insufficiency requiring prolonged hemodialysis delayed cranial nerve deficits – cranial nerves II, V, VII, VIII, IX, X, and XII – related to calcium oxalate crystal deposition – may be observed on MRI

62. Delayed symptoms All these injuries slowly resolve last as long as several months particularly after severe encephalopathy or profound acidemia with reported arterial pH as low as 6.46